The key goal of this study is to develop the cat as a practical model to study organophosphorus-induced delayed neurotoxicity. Most organophosphorus esters are direct inhibitors or are rapidly converted to inhibitors of acetylcholinesterase. Some of these compounds produce a more persistent effect: delayed neurotoxicity. In humans and sensitive animals, organophosphorus ester-induced delayed neurotoxicity results in a flaccid paresis which develops distally in the legs and spreads to the hands and thighs. In the later stages, symptoms of spinal cord injury such as spasticity and ataxia become evident as the symptoms of peripheral neuropathy recede. Some species are susceptible (cats, dogs, cows and chickens) while others (rodents and some primates) are not. The adult chicken has been used as the test animal of choice to study delayed neurotoxicity. Tri-o-cresyl phosphate (TOCP) was the first compound to cause delayed neurotoxicity in humans and animals. O-ethyl O-4 nitrophenyl phenylphosphonothioate (EPN) is a neurotoxic insecticide. In this study, the delayed neurotoxic effect of EPN and TOCP is being investigated in the cat. Several parameters are correlated: the clinical condition, neurological examination, electrophysiological changes, electromyographic measurements, histopathological alterations in the central and peripheral nervous system, biochemical parameters such as cholinesterases and acid phosphatase in the brain and plasma and neurotoxic esterase in the brain of cats dermally treated with EPN and TOCP. Furthermore, these results will be correlated with the pharmacokinetic and metabolic studies of a single or daily dermal doses of (14C)EPN.